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Toxicol Lett. 2017 May 5;273:26-35. doi: 10.1016/j.toxlet.2017.03.010. Epub 2017 Mar 21.

Transcriptome analysis of airborne PM2.5-induced detrimental effects on human keratinocytes.

Author information

1
Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea.
2
Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea; College of Veterinary Medicine, Seoul National University, Seoul, 151-742 Republic of Korea.
3
Macrogen Inc., Seoul, 08511, Republic of Korea.
4
College of Veterinary Medicine, Seoul National University, Seoul, 151-742 Republic of Korea.
5
Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea. Electronic address: TRLee@amorepacific.com.
6
Amorepacific Corporation R&D Center, Yongin-si, Gyeonggi-do, 446-729, Republic of Korea. Electronic address: biopang@amorepacific.com.

Abstract

Ambient air pollution is becoming more severe worldwide, posing a serious threat to human health. Fine airborne particles of particulate matter (PM2.5) show higher cytotoxicity than other coarse fractions. Indeed, PM2.5 induces cardiovascular or respiratory damage; however, few studies have evaluated the detrimental effect of PM2.5 to normal human skin. We used a next-generation sequencing-based (RNA-Seq) method with transcriptome and Gene Ontology (GO) enrichment analysis to determine the harmful influences of PM2.5 on human normal epidermal keratinocytes. DAVID analysis showed that the most significantly enriched GO terms were associated with epidermis-related biological processes such as "epidermis development (GO: 0008544)" and "keratinocyte differentiation (GO: 0030216)", suggesting that PM2.5 has some deleterious effects to the human epidermis. In addition, Ingenuity Pathway Analysis predicted inflammation-related signaling as one of the major PM2.5-induced signaling pathways, and pro-inflammatory cytokines as upstream regulators with symptoms similar to psoriasis as downstream effects. PM2.5 caused considerable changes in the expression of pro-inflammatory cytokines and psoriatic skin disease-related genes, might lead to epidermal dysfunctions. Our results might help to understand the mechanism of air pollution-induced skin barrier perturbation and contribute to the development of a new strategy for the prevention or recovery of the consequent damage.

KEYWORDS:

Human normal keratinocytes; Next-generation sequencing; Particulate matter

PMID:
28341207
DOI:
10.1016/j.toxlet.2017.03.010
[Indexed for MEDLINE]

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